A variety of pathological and accidental causes give rise to damage to the cornea of the eye. Corneal ulceration and resultant scarring are among the most frequent causes of loss of vision worldwide. Ulceration can result from infections, as with Pseudomonas, Staghglococcus, Herpes, and fungi, as well as from chemical and thermal burns, including sometimes after thermokeratoplasty. Ulceration can also occur in association with severe vitamin A and protein deficiency (keratomalacia); in certain "dry eye" conditions, and in neuroparalytic keratitis; in eyes of patients with autoimmune disease apparently limited to the cornea (Mooren's ulcer), and in association with known systemic autoimmune disorders, like lupus erythematosus and Wegener's granulomatosis, and possible autoimmune diseases like rheumatoid arthritis. Ulceration sometimes progresses to actual perforation with the formation of synechiae between iris and cornea, secondary glaucoma, and even blindness due to death of the optic nerve. Usually, however, after serious insult to the cornea and enzymatic erosion of the stromal matrix, ulceration is arrested, and the cornea, like injured skin, forms scar tissue which scatters light, causing loss of visual acuity. Other mechanical damage can also occur to the cornea, as from scratches or punctures by foreign objects. For these and a variety of other reasons, the corneal portions of eyes must be surgically repaired or replaced.
As ulceration (resulting in scarring and consequent loss of visual acuity) is a primary concern in most corneal damage, either as the result of one of the above diseases or as a side effect of other traumatic injury to the eye, prevention or mitigation of ulceration in the above situations will usually minimize or eliminate scarring and the attendant loss of vision. It is believed that ulceration is the result of local release of proteolytic enzymes--collagenase and other proteases. Likely, these enzymes are released by polymorphonuclear leukocytes, although other cell types may also contribute. Upon severe inflammation of the anterior segment, leukocytes leak out from the dilated conjunctival capillaries into the tear film. If there is an epithelial defect of the cornea, the leukocytes appear to attach to the naked stromal surface, and there release their proteolytic enzymes, causing digestion of the corneal tissue. Mechanical protection of the epithelial defect, as by gluing on a contact lens, appears to be effective in preventing such ulceration. See generally, C. Dohlman, "Biology of Complications following Keratoprosthesis," Cornea 2: 175-76 (1983); and M. Berman, "Collagenase and Corneal Ulceration," in Collagenase in Normal and Pathological Tissue, D. Wooley and J. Evanson, eds., John Wiley & Sons, Ltd., New York (1980). This technique is not always possible or effective, however, particularly in the case of keratoprostheses, as typical adhesives usable in vivo, such as cyanoacrylate, form only a temporary bond at best, which is eventually degraded by tears and/or necrosis.
Corneal transplants are often necessary for a variety of reasons, including repair of an opacified cornea after an ulcer has healed by forming scar tissue. Such transplants have become quite common in the United States, particularly with the advent of microsurgery. Unfortunately, donor corneas are very difficult to obtain. A cornea to be donated must be employed, if at all, within a matter of days or weeks from the time of death of the donor. Although eye banks have been organized throughout the United States, one cannot rely upon the availability of a donor at the time it is needed for a transplant operation. As a result, vision which could have been wholly or partially restored in many patients often is lost permanently. Furthermore, some diseases are not amenable to standard corneal transplants, and corneal transplants carry the constant risk of transmission of diseases carried in the transplanted tissue, including leukemia, syphilis, and Acquired Immunodeficiency Syndrome (AIDS). See Fuji Kawa, et. al., "Human T-Cell Leukemia/Lymphotrophic Virus Type III in the Conjunctival Epithelium of Patient with AIDS," 100 Amer. J. Opthal. 507 (Oct. 1985); Pepose et. al., "The Impact of the AIDS Epidemic on Corneal Transplantation," 100 Amer. J. Opthal. 610 (Oct. 1985).
Attempts have been made in the past to utilize artificial materials for corneal transplants. Representative of such attempts are those reported in Barraquer, Queratomileusis y Queragofaquia, Instituto Barraquer de America Bogata, Col. (1980); U.S. Pat. No. 3,945,054, issued Mar. 23, 1976, Fedorov, et. al., "Through Corneal Prosthesis and Method of Installing Same"; and U.S. Pat. No. 3,458,870, issued Aug. 5, 1969, W. Stone, Jr., "Artificial Corneal Implants Having a Removable Lens Member."
For the most part, the implantation of artificial corneal materials has been at best a temporary stop gap measure taken to seal the anterior chamber of the eye for a period of time until a donor cornea could be located for transplantation. As with other parts of the human body, the eye tends to reject and eject or extrude foreign materials during the healing process, with the result that the implantation of artificial corneas generally leads to loss by extrusion of the device, to further eye damage and to leakage of aqueous humor from the anterior chamber. Attempts to affix artificial corneas to the cornea by adhesive typically fail because the living cells contacted by adhesive eventually die and slough off (necrosis), destroying the adhesive seal. Thus, the prior art devices have relied on elaborate mechanical attachment methods which are fraught with continued need for surgical revision, and have had short-lived, limited success.